Key result
Calcineurin inhibitors are associated with arterial hypertension in 50-80% of transplanted patients through mechanisms including impaired renal function, endothelial dysfunction, and RAAS activation.
Why the study?
What are the mechanisms of calcineurin inhibitor-induced arterial hypertension in solid organ transplant recipients?
What are the mechanisms of calcineurin inhibitor-induced arterial hypertension in solid organ transplant recipients?
Calcineurin inhibitors induce arterial hypertension in 50-80% of solid organ transplant recipients through multiple mechanisms including RAAS activation, endothelial dysfunction, and renal sodium retention.
Requires vigilant BP monitoring in CNI-treated transplant recipients; leaves open mechanism-specific interventions pending prospective data.
Arterial hypertension is an established risk factor for cardiovascular complications. Since the introduction of calcineurin inhibitors (CNI), аrterial hypertension is observed in 50-80% of transplanted patients. Arterial hypertension and transplantation are closely linked, and its association may promote impaired graft and overall survival. We summarize the main mechanisms involved in the genesis of CNI-induced hypertension as follows: impaired renal function with the sodium retaining, endothelial dysfunction, renin-angiotensin-aldosterone system and sympathetic activation, production of vasoconstrictor substances, activation the renal Na+/Cl--cotransporter. Attention is focused on the dose-dependent increase in arterial pressure and the need for further study of the intensity of the pro-hypertensive effect of various calcineurin inhibitors.
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Космачева et al. (2017) conducted a review in Arterial hypertension in recipients of solid organs. Calcineurin inhibitors was evaluated on Arterial hypertension. Calcineurin inhibitors are associated with arterial hypertension in 50-80% of transplanted patients through mechanisms including impaired renal function, endothelial dysfunction, and RAAS activation.
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